Cirrhosis laboratory findings: Difference between revisions
No edit summary |
|||
| Line 4: | Line 4: | ||
{{CMG}} ; {{AE}} {{ADI}} | {{CMG}} ; {{AE}} {{ADI}} | ||
==Overview== | ==Overview== | ||
A range of laboratory values need to be obtained in the evaluation of cirrhosis, both to determine the severity of the disease, and to determine the causative factor. Liver function tests, complete blood counts, basic metabolic panels and coagulation factors are standard in the evaluation of cirrhosis. More specific testing for markers and serum enzymes can be done when certain genetic causes and etiologies are suspected. | |||
==Laboratory Findings== | ==Laboratory Findings== | ||
Revision as of 14:24, 7 September 2012
|
Cirrhosis Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case studies |
|
Cirrhosis laboratory findings On the Web |
|
American Roentgen Ray Society Images of Cirrhosis laboratory findings |
|
Risk calculators and risk factors for Cirrhosis laboratory findings |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Aditya Govindavarjhulla, M.B.B.S. [2]
Overview
A range of laboratory values need to be obtained in the evaluation of cirrhosis, both to determine the severity of the disease, and to determine the causative factor. Liver function tests, complete blood counts, basic metabolic panels and coagulation factors are standard in the evaluation of cirrhosis. More specific testing for markers and serum enzymes can be done when certain genetic causes and etiologies are suspected.
Laboratory Findings
The following findings are typical in cirrhosis:
- Aminotransferases - AST and ALT are moderately elevated, with AST > ALT, however, normal aminotransferases do not preclude cirrhosis.
- Alcoholic liver disease - AST and ALT are both elevated but less than 300 IU/L with a AST:ALT ratio > 2.0
- Alkaline phosphatase - It is elevated but usually less than two to three times the upper limit. Patients with primary biliary cirrhosis and primary sclerosing cholangitis may have higher levels.
- GGT -- correlates with AP levels. It is typically much higher in chronic liver disease from alcohol.
- Bilirubin - may elevate as cirrhosis progresses.
- Albumin - levels fall as the synthetic function of the liver declines with worsening cirrhosis since albumin is exclusively synthesized in the liver.
- Prothrombin time - increases since the liver synthesizes clotting factors.
- Globulins - increase due to shunting of bacterial antigens away from the liver to lymphoid tissue which induces immunoglobulin production.
- Serum sodium- hyponatremia due to inability to excrete free water resulting from high levels of ADH and aldosterone.
- Thrombocytopenia - due to both congestive splenomegaly as well as decreased thrombopoietin from the liver, however this rarely results in a platelet count < 50,000/mL.
- Leukopenia and neutropenia - due to splenomegaly with splenic margination.
- Anemia - multifactorial in origin.
- Acute and chronic GI bleeding
- Folate deficiency
- Direct toxicity of alcohol
- Hypersplenism
- Bone marrow suppression
- Anemia of chronic disease
- Hemolysis
- Coagulation defects - the liver produces most of the coagulation factors and thus coagulopathy correlates with worsening liver disease.
There is now a validated and patented combination of 6 of these markers as non-invasive biomarkers of fibrosis (and so of cirrhosis) : FibroTest.[1]
Other laboratory studies performed in newly diagnosed cirrhosis may include:
- Serology for hepatitis viruses.
- Autoantibodies
- ANA - present in autoimmune hepatitis
- Anti-smooth muscle antibody - present in autoimmune hepatitis
- Anti-mitochondrial antibody - present in primary biliary cirrhosis
- Anti-LKM
- Total iron, TIBC, transferrin saturation, and ferritin - elevated totat iron, reduced TIBC, elevated transferrin saturation, and elevated ferritin in hemochromatosis.
- Serum ceruloplasmin- low in Wilson's disease
- Immunoglobulin levels (IgG, IgM, IgA) - these are non-specific but may assist in distinguishing various causes.
- Chronic hepatitis B - Chronic hepatitis B can be diagnosed with detection of HBsAG > 6 months after initial infection. HBeAG and HBV DNA are determined to assess whether or not patients will need antiviral therapy.
- Serum protein electrophoresis - alpha-1 band absent in alpha-1 antitrypsin deficiency.
- Cholesterol and glucose
- Alpha 1-antitrypsin - reduced in alpha-1 antitrypsin deficiency.
References
- ↑ Halfon P, Munteanu M, Poynard T (2008). "FibroTest-ActiTest as a non-invasive marker of liver fibrosis". Gastroenterol Clin Biol. 32 (6): 22–39. doi:10.1016/S0399-8320(08)73991-5. PMID 18973844.